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Correction to: The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia

  • Qianqian Liu
  • Hongye Ma
  • Xiuhua Sun
  • Bing Liu
  • Yang Xiao
  • Shimeng Pan
  • Huimin Zhou
  • Weijie Dong
  • Li JiaEmail author
Open Access
Correction
  • 33 Downloads

Correction to: J Exp Clin Cancer Res (2019) 38:199

https://doi.org/10.1186/s13046-019-1208-x

In the original publication of this article [1], there is a mistake in Fig. 4e.

The corrected Fig. 4e should be:
Fig. 1

Upregulation of ST6GAL1 promotes proliferation and chemoresistance in T-ALL cell lines (a) qRT-PCR and western blot were carried out to detect ST6GAL1 levels. b The expression of FITC-SNA was dertermined. c The viability of cells transfected with ST6GAL1 was determined by CCK8 assay at 0, 24, 48, 72 and 96 h. d Enhanced ST6GAL1 facilitated colony formation. e Ki67 expression was observed by immunoflourescence, red fluorescence: Ki67, blue fluorescence: DAPI. f CCK8 assays were used to measure the resistance to ADR, VCR and Pacliatxel. The absorbance was measured at 450 nm. g The IC50 values were calculated. h Relative molecular expression of key caspase-dependent apoptosis was analyzed by western blot. i The apoptosis rate of different treated cells was analyzed by FCM. ST6GAL1 upregulation inhibited cells survival in response to ADR. j Effects of ST6GAL1 upregulation on tumor growth were shown in vivo. k ST6GAL1 and Ki67 expression was observed by IHC staining. Data were means ± SD of triplicate determinants (*P < 0.05)

Reference

  1. 1.
    Liu Q, et al. The regulatory ZFAS1/miR-150/ST6GAL1 crosstalk modulates sialylation of EGFR via PI3K/Akt pathway in T-cell acute lymphoblastic leukemia. J Exp Clin Cancer Res. 2019;38:199.CrossRefGoogle Scholar

Copyright information

© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Authors and Affiliations

  • Qianqian Liu
    • 1
  • Hongye Ma
    • 2
  • Xiuhua Sun
    • 3
  • Bing Liu
    • 1
  • Yang Xiao
    • 1
  • Shimeng Pan
    • 1
  • Huimin Zhou
    • 4
  • Weijie Dong
    • 5
  • Li Jia
    • 1
    Email author
  1. 1.College of Laboratory Medicine, Dalian Medical UniversityDalianChina
  2. 2.Department of Clinical LaboratoryBeijing Hospital of Traditional Chinese Medicine Affiliated to Capital University of Medicine SciencesBeijingChina
  3. 3.Department of Medicine OncologySecond Affiliated Hospital of Dalian Medical UniversityDalianChina
  4. 4.Department of MicrobiologyDalian Medical UniversityDalianChina
  5. 5.Department of BiochemistryDalian Medical UniversityDalianChina

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